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1.
J Arthroplasty ; 33(8): 2412-2416, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29656963

RESUMO

BACKGROUND: Hospital length of stay is a major driver of cost in the total hip arthroplasty (THA) episode of care, and as a result, significant efforts are being made to minimize it. This study aims to assess the utility of the Outpatient Arthroplasty Risk Assessment (OARA) screening tool in accurately identifying patients for safe and early discharge after THA. METHODS: A retrospective review was conducted on 332 consecutive patients who underwent primary THA at a single tertiary academic center. Patients were evaluated using the OARA score, a tool that has been proposed to identify patients who can safely undergo early discharge after THA. The validity of these claims was assessed by analyzing the OARA score's positive and negative predictive values for high vs low OARA scores between patients enrolled in our (1) same-day discharge (SDD) and 2) next-day discharge (NDD) pathways. RESULTS: When comparing the utility of the OARA score in accurately predicting length of stay, the OARA score demonstrated a (1) higher, but constant, positive predictive value for discharge on postoperative day (POD) 0 for SDD (86.1%) than POD1 for NDD (35.5%) and (2) lower negative predictive value for discharge on POD0 (23.1%) for SDD than POD1 for NDD (86.1%). CONCLUSION: The OARA score was developed to risk-stratify patients who can safely undergo SDD or NDD after THA. In this study, the OARA score was a highly predictive tool in identifying NDD patients at risk for failure of discharge by POD1.


Assuntos
Artroplastia de Quadril/estatística & dados numéricos , Artroplastia do Joelho/estatística & dados numéricos , Alta do Paciente , Medição de Risco/métodos , Idoso , Algoritmos , Artroplastia de Quadril/efeitos adversos , Feminino , Humanos , Tempo de Internação , Masculino , Pessoa de Meia-Idade , Pacientes Ambulatoriais/estatística & dados numéricos , Período Pós-Operatório , Valor Preditivo dos Testes , Estudos Retrospectivos
2.
Circ Arrhythm Electrophysiol ; 11(1): e005914, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-29311162

RESUMO

BACKGROUND: Myocardial, transient, outward currents, Ito, have been shown to play pivotal roles in action potential (AP) repolarization and remodeling in animal models. The properties and contribution of Ito to left ventricular (LV) repolarization in the human heart, however, are poorly defined. METHODS AND RESULTS: Whole-cell, voltage-clamp recordings, acquired at physiological (35°C to 37°C) temperatures, from myocytes isolated from the LV of nonfailing human hearts identified 2 distinct transient currents, Ito,fast (Ito,f) and Ito,slow (Ito,s), with significantly (P<0.0001) different rates of recovery from inactivation and pharmacological sensitives: Ito,f recovers in ≈10 ms, 100× faster than Ito,s, and is selectively blocked by the Kv4 channel toxin, SNX-482. Current-clamp experiments revealed regional differences in AP waveforms, notably a phase 1 notch in LV subepicardial myocytes. Dynamic clamp-mediated addition/removal of modeled human ventricular Ito,f, resulted in hyperpolarization or depolarization, respectively, of the notch potential, whereas slowing the rate of Ito,f inactivation resulted in AP collapse. AP-clamp experiments demonstrated that changes in notch potentials modified the time course and amplitudes of voltage-gated Ca2+ currents, ICa. In failing LV subepicardial myocytes, Ito,f was reduced and Ito,s was increased, notch and plateau potentials were depolarized (P<0.0001) and AP durations were prolonged (P<0.001). CONCLUSIONS: Ito,f and Ito,s are differentially expressed in nonfailing human LV, contributing to regional heterogeneities in AP waveforms. Ito,f regulates notch and plateau potentials and modulates the time course and amplitude of ICa. Slowing Ito,f inactivation results in dramatic AP shortening. Remodeling of Ito,f in failing human LV subepicardial myocytes attenuates transmural differences in AP waveforms.


Assuntos
Insuficiência Cardíaca/metabolismo , Ventrículos do Coração/metabolismo , Miocárdio/metabolismo , Potássio/metabolismo , Feminino , Insuficiência Cardíaca/patologia , Insuficiência Cardíaca/fisiopatologia , Ventrículos do Coração/patologia , Humanos , Masculino , Potenciais da Membrana/fisiologia , Pessoa de Meia-Idade , Miocárdio/patologia , Técnicas de Patch-Clamp , Canais de Potássio/metabolismo
4.
Cell Rep ; 19(3): 532-544, 2017 04 18.
Artigo em Inglês | MEDLINE | ID: mdl-28423317

RESUMO

The resurgent component of voltage-gated Na+ (Nav) currents, INaR, has been suggested to provide the depolarizing drive for high-frequency firing and to be generated by voltage-dependent Nav channel block (at depolarized potentials) and unblock (at hyperpolarized potentials) by the accessory Navß4 subunit. To test these hypotheses, we examined the effects of the targeted deletion of Scn4b (Navß4) on INaR and on repetitive firing in cerebellar Purkinje neurons. We show here that Scn4b-/- animals have deficits in motor coordination and balance and that firing rates in Scn4b-/- Purkinje neurons are markedly attenuated. Acute, in vivo short hairpin RNA (shRNA)-mediated "knockdown" of Navß4 in adult Purkinje neurons also reduced spontaneous and evoked firing rates. Dynamic clamp-mediated addition of INaR partially rescued firing in Scn4b-/- Purkinje neurons. Voltage-clamp experiments revealed that INaR was reduced (by ∼50%), but not eliminated, in Scn4b-/- Purkinje neurons, revealing that additional mechanisms contribute to generation of INaR.


Assuntos
Potenciais de Ação/fisiologia , Ativação do Canal Iônico , Atividade Motora/fisiologia , Equilíbrio Postural/fisiologia , Células de Purkinje/metabolismo , Sódio/metabolismo , Subunidade beta-4 do Canal de Sódio Disparado por Voltagem/deficiência , Envelhecimento , Animais , Animais Recém-Nascidos , Diferenciação Celular , Separação Celular , Feminino , Deleção de Genes , Técnicas de Silenciamento de Genes , Marcação de Genes , Masculino , Camundongos Endogâmicos C57BL , Neurônios/citologia , Neurônios/metabolismo , Técnicas de Patch-Clamp , Subunidade beta-4 do Canal de Sódio Disparado por Voltagem/metabolismo
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